Peroxisome proliferator-activated receptor-gamma targeting nanomedicine promotes cardiac healing after acute myocardial infarction by skewing monocyte/macrophage polarization in preclinical animal models

Terabe, Masaki; Matoba, Tetsuya; Nakano, Yukiko; Okahara, Arihide; Fujiwara, Masaki; Koga, J.; Nakano, K.; Tsutsui, Hiroyuki; Egashira, Kensuke

doi:10.1093/cvr/cvy200

Cited by 86 publications

(58 citation statements)

References 45 publications

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“…Lee and colleagues found that YAP/TAZ participates in the regulation of 135 genes in macrophages, of which 66 were closely related to cell development, differentiation, metabolism, and immunity, including PPARg, myoblast determination protein (MyoD), the zinc finger of the cerebellum 1 (Zic1), and lymphocyte function-associated antigen 1 (LF-A1) (87). The transcription factor PPARg has also been reported to modulate the polarization and inflammatory responses of macrophages (42,43,93). YAP/TAZ plays a crucial role in the biological activity of macrophages.…”

Section: Yap/taz In Regulating Macrophagesmentioning

confidence: 99%

The Emerging Role of YAP/TAZ in Tumor Immunity

Pan

Tian²,

Cao

et al. 2019

Molecular Cancer Research

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Yes-associated protein (YAP)/WW domain-containing transcription regulator 1 (TAZ) is an important transcriptional regulator and effector of the Hippo signaling pathway that has emerged as a critical determinant of malignancy in many human tumors. YAP/TAZ expression regulates the cross-talk between immune cells and tumor cells in the tumor microenvironment through its influence on T cells, myeloid-derived suppressor cells, and macrophages. However, the mechanisms underlying these effects are poorly understood. An improved understanding of the role of YAP/TAZ in tumor immunity is essential for exploring innovative tumor treatments and making further breakthroughs in antitumor immunotherapy. This review primarily focuses on the role of YAP/TAZ in immune cells, their interactions with tumor cells, and how this impacts on tumorigenesis, progression, and therapy resistance.

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Section: Yap/taz In Regulating Macrophagesmentioning

confidence: 99%

The Emerging Role of YAP/TAZ in Tumor Immunity

Pan

Tian²,

Cao

et al. 2019

Molecular Cancer Research

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“…Peripheral monocytes/macrophages and cardiac‐resident macrophages migrate to the infarct and border region, differentiate into M1 macrophages, and exacerbate cardiac function. Thereafter, entering the inflammation resolution stage, the dominant macrophage populations of myocardial tissues become reparative M2 macrophages that accelerate cardiac repair (Gombozhapova et al, ; Tokutome et al, ). Inflammation from M1 macrophages is an essential component of early ventricle remodeling, and prolonged inflammation may damage the physiology of the left ventricle (LV) by raising LV expansion and redundant scar transformation (Ben‐Mordechai et al, ; Gombozhapova et al, ).…”

Section: Introductionmentioning

confidence: 99%

C1q/TNF‐related protein‐9 promotes macrophage polarization and improves cardiac dysfunction after myocardial infarction

Liu

Yin

et al. 2019

Journal Cellular Physiology

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The timely regulation of inflammatory M1 macrophage polarization toward regenerative M2 macrophages suggests the possibility of immunotherapy after myocardial infarction (MI). C1q/TNF‐related protein‐9 (CTRP9) has anti‐inflammatory effects and can ameliorate heart function in mice after long‐term myocardial infarction. The role of CTRP9 in macrophage polarization remains completely unclear. This study determined whether CTRP9 can preserve post‐MI early cardiac function through the regulation of macrophage polarization. In the present study, an adenovirus‐delivered CTRP9 supplement promoted macrophage polarization at Day 3 post MI and improved cardiac function at Day 7 post MI. Pretreatment with gCTRP9 promoted the M1 to M2 polarization transition and attenuated inflammation after lipopolysaccharide + interferon‐γ stimulation; the effects were partly abrogated by the adenosine monophosphate kinase (AMPK) inhibitor compound C and were obviously reinforced by pyrrolidine dithiocarbamate, a nuclear factor‐κB (NF‐κB) inhibitor. Meanwhile, CTPR9 markedly reduced the expression of toll‐like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF‐κB p65 phosphorylation by promoting AMPK phosphorylation in vivo and in vitro. Moreover, the competitive binding of gCTRP9 and LPS to the myeloid differentiation protein 2 (MD2)/TLR4 complex was associated with direct binding to MD2, thereby inhibiting the downstream signaling molecule MyD88. Taken together, we demonstrated that CTRP9 improved post‐MI early cardiac function, at least in part, by modulating M1/M2 macrophage polarization, largely via the TLR4/MD2/MyD88 and AMPK‐NF‐κB pathways.

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“…[140] PPAR activation in monocytes/macrophages, obtained by targeting a PPAR agonist to phagocytes with a nanocarrier, achieved promising results in a preclinical model of myocardial infarction. [141] Modulation of PPAR activity via NM may therefore be developed as a novel therapeutic strategy for anti-inflammatory and pro-healing effects.…”

Section: Nanomaterials and Activation Of Innate Immune Genes/factorsmentioning

confidence: 99%

Addressing Nanomaterial Immunosafety by Evaluating Innate Immunity across Living Species

Boraschi

Alijagić

Auguste

et al. 2020

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The interaction of a living organism with external foreign agents is a central issue for its survival and adaptation to the environment. Nanosafety should be considered within this perspective, and it should be examined that how different organisms interact with engineered nanomaterials (NM) by either mounting a defensive response or by physiologically adapting to them. Herein, the interaction of NM with one of the major biological systems deputed to recognition of and response to foreign challenges, i.e., the immune system, is specifically addressed. The main focus is innate immunity, the only type of immunity in plants, invertebrates, and lower vertebrates, and that coexists with adaptive immunity in higher vertebrates. Because of their presence in the majority of eukaryotic living organisms, innate immune responses can be viewed in a comparative context. In the majority of cases, the interaction of NM with living organisms results in innate immune reactions that eliminate the possible danger with mechanisms that do not lead to damage. While in some cases such interaction may lead to pathological consequences, in some other cases beneficial effects can be identified.

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Peroxisome proliferator-activated receptor-gamma targeting nanomedicine promotes cardiac healing after acute myocardial infarction by skewing monocyte/macrophage polarization in preclinical animal models

Abstract: Nanoparticle-mediated targeting of pioglitazone to inflammatory monocytes protected the heart from IR injury and cardiac remodeling by antagonizing monocyte/macrophage-mediated acute inflammation and promoting cardiac healing after AMI.

Cited by 86 publications

References 45 publications

The Emerging Role of YAP/TAZ in Tumor Immunity

The Emerging Role of YAP/TAZ in Tumor Immunity

C1q/TNF‐related protein‐9 promotes macrophage polarization and improves cardiac dysfunction after myocardial infarction

Addressing Nanomaterial Immunosafety by Evaluating Innate Immunity across Living Species

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